Postpartum psychological distress after emergency team response during childbirth

Purpose: To evaluate the feasibility and acceptability of a protocol determining the relationship between emergency team response (ETR) during childbirth and acute stress disorder (ASD) and post-traumatic stress disorder (PTSD) symptoms.

Methods: In a prospective, observational, cohort design, women experiencing ETR during childbirth were approached and recruited on postpartum day-1 and followed for six weeks. Demographics, obstetric and birth characteristics, ASD scores and PTSD scores (by Impact of Events Scale, IES and PCL-civilian) were recorded. Recruitment and retention rates were recorded, and scores were compared to women who did not experience ETR.

Results: Three hundred sixty-nine were approached and 249 were enrolled (67.5% recruitment rate). One hundred twenty-five completed all procedures (50.2% retention). Twenty experienced ETR (3.5% event rate), 12 enrolled (60.0% recruitment rate) and 8 completed the study (66.7% retention). The ETR group had higher PCL and IES scores (PCL: ETR median 12, non-ETR median 2, p?=?.08; IES: ETR median 22.5, non-ETR median 20, p?=?.08). ASD scores were similar between groups.

Conclusions: Methodology investigating the link between ETR and postpartum psychological distress is feasible and acceptable. A relationship between ETR and PTSD symptoms appears to exist, with ETR being associated with higher PTSD scores compared to non-ETR childbirths. Methods that incorporate awareness of the unique concerns of vulnerable populations are needed.     

HIV Testing in the Nation's Opioid Treatment Programs, 2005–2011: The Role of State Regulations

ObjectiveTo identify the extent to which clients in a national sample of opioid treatment programs (OTPs) received HIV testing in 2005 and 2011; to examine relationships between state laws for informed consent and pretest counseling and rates of HIV testing among OTP clients.Data SourceData were collected from a nationally representative sample of OTPs in 2005 (n = 171) and 2011 (n = 200).Study DesignRandom-effects logit and interval regression analyses were used to examine changes in HIV testing rates and the relationship of state laws to HIV testing among OTPs.Data CollectionData on OTP provision of HIV testing were collected in phone surveys from OTP managers; data also were collected on state laws for HIV testing.Principal FindingsThe percentage of OTPs offering HIV testing decreased significantly from 93 percent in 2005 to 64 percent in 2011. Similarly, the percentage of clients tested decreased from an average of 41 percent in 2005 to 17 percent in 2011. OTPs located in states whose laws do not require pretest counseling and that use opt-out consent were more likely to provide HIV testing and to test higher percentages of clients.ConclusionsThe results show the need to increase HIV testing among OTP clients; the results also underscore the beneficial possibilities of dropping pretest counseling as a requirement for HIV testing and of using the opt-out approach to informed consent for testing.     

Evaluation of 5-(Trifluoromethyl)-1,2,4-oxadiazole-Based Class IIa HDAC Inhibitors for Huntington’s Disease

Using an iterative structure–activity relationship driven approach, we identified a CNS-penetrant 5-(trifluoromethyl)-1,2,4-oxadiazole (TFMO, 12) with a pharmacokinetic profile suitable for probing class IIa histone deacetylase (HDAC) inhibition in vivo. Given the lack of understanding of endogenous class IIa HDAC substrates, we developed a surrogate readout to measure compound effects in vivo, by exploiting the >100-fold selectivity compound 12 exhibits over class I/IIb HDACs. We achieved adequate brain exposure with compound 12 in mice to estimate a class I/IIb deacetylation EC₅₀, using class I substrate H4K12 acetylation and global acetylation levels as a pharmacodynamic readout. We observed excellent correlation between the compound 12 in vivo pharmacodynamic response and in vitro class I/IIb cellular activity. Applying the same relationship to class IIa HDAC inhibition, we estimated the compound 12 dose required to inhibit class IIa HDAC activity, for use in preclinical models of Huntington’s disease.